Idiopathic anterior uveitis in man is characterized by a breakdown of the blood-aqueous barrier which is acute and often recurrent. Left untreated, it can frequently lead to secondary glaucoma. Since currently available objective measures of ocular flammation usually necessitate undesirable invasive procedures such as paracentesis, clinical assessment of the severity of anterior uveitis, and its response to therapy, has relied heavily upon subjective grading of such parameters as iris hyperemia, flare and cells. A major aim of the proposed studies is adaptation of the technique of aqueous fluorophotometry to the objective, but non-invasive measure of anterior segment inflammation. Eventual direct, clinical application of the procedure is our long-range goal. Following preliminary studies in rabbits, aqueous fluorophotometry will be used for correlative studies of a Shigella endotoxin-induced model of anterior uveitis in monkeys. By taking advantage of recently available fluorescein-labelled ultrastructural tracers, we will be able to correlate fluorophotometric estimates of the severity of anterior uveitis with results of ultrastructural tracer studies on the same eyes. Additional studies, using the above correlative procedures, in conjunction with the freeze-fracture technique, will examine the process of re-establishment of the blood-aqueous barrier during resolution of anterior uveitis, both with and without treatment using steroidal and non-steroidal anti-inflammatory agents. Particular emphasis will be given to the mechanisms involved in the reassembly of tight junction, which constitute the anatomic equivalent of the blood-aqueous barrier. Incomplete or faulty barrier reformation, after uveitis, could contribute to recurrence. Thus, knowledge of the process of barrier reformation may be critical to an understanding of recurrent anterior uveitis in man. Further insights into the etiology of recurrent anterior uveitis will result from electron microscopic and freeze-fracture studies comparing the induced disease model in monkeys with a naturally occurring model in horses termed periodic equine ophthalmia.